The long-range goal of this project is to determine how the human central nervous system (CNS) coordinates voluntary movement and ultimately to use this information to develop treatments for motor disorders, such as stroke. The goal of the research proposed in this application is to determine how proprioception at the receptor level-in this case, the muscle spindle-leads to perception. The central hypothesis to be investigated is that, in active movement, the primary source of proprioceptive input is muscle spindles in the lengthening, "antagonist" muscles, rather than muscle spindles in the contracting, "agonist" muscles. Three specific aims are addressed: Specific Aim 1 is to contrast the information signaled by agonist and antagonist muscle spindles to determine which of these populations provides the CNS with the most accurate information about limb position and movement. Unlike agonist muscle spindles, little is known about how antagonist muscle spindles respond to active joint rotation. We will characterize how agonist and antagonist muscle spindles signal joint position and movement to test the hypothesis that the CNS uses the input from both populations, but that the information provided by antagonist muscle spindles is the most accurate. Specific Aim 2 is to investigate how antagonist muscle spindles encode position and movement variables, to inform the CNS of the location and movement of the limbs in space. The proposed experiments are designed to test the hypothesis that, during a movement, antagonist muscle spindles signal the CNS information about the starting position, movement velocity, and limb position during movement by three distinctive features within the firing pattern. Specific Aim 3 is to characterize the influence of fusimotor input on antagonist muscle spindles. Past research on agonist muscle spindles has failed to explain why the CNS activates the fusimotor system during voluntary movement. The proposed experiments are designed to test the hypothesis that fusimotor input increases the precision with which antagonist muscle spindles signal limb position and movement during precise movements and during motor learning, but that fusimotor input does not decrease the precision of signaling from antagonist muscle spindles during loaded movements.